Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Neonatal”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 613 records · Page 34Linked to original sources
PubMed1996

G3P2 rotaviruses causing diarrhoeal disease in neonates differ in VP4, VP7 and NSP4 sequence from G3P2 strains causing asymptomatic neonatal infection.

During longitudinal epidemiological studies of rotavirus infections in children in Melbourne, Australia human G3P2 rotavirus strains causing asymptomatic or symptomatic infections have been identified. Eleven strains (AS strains) associated with asymptomatic infection of newborn babies from 1974-1984, and five strains (S strains) associated with symptomatic infection of newborn babies (4) or a 22 week old infant (1) during 1980-1986 were studied. The entire nucleotide sequences of genes coding for VP4, VP7, NSP4 and VP6 were derived for representative AS and S strains. The nucleotide sequences of neutralization epitope regions present on the outer capsid proteins VP4 and VP7 (regions C and F) showed extensive conservation of nucleotide and deduced amino acid sequence in all strains. Minor variations were observed over the 12 year period in VP7 epitope regions A and B in some strains. Specific conserved amino acids differences between the asymptomatic and symptomatic strains were observed in the genes encoding VP4 at aa133 and 303 (asparagine or threonine) and 380 (serine or isoleucine), VP7 at aa27 (threonine or isoleucine), aa29 (isoleucine or threonine), aa42 (valine or alanine) and aa238 (asparagine or aspartic acid/serine) and NSP4 at aa135 (isoleucine or valine). No amino acid changes were identified in gene 6. The observed amino acid differences occurred in proteins that have been implicated in virulence, and correlate with differences in clinical symptoms of infants infected with these strains. These results permit speculation about the genetic basis for virulence of human strains.

Amino Acid Sequence↗
PubMed2006

Twin differences in birth weight: the effects of genotype and prenatal environment on neonatal and post-neonatal mortality.

There is much evidence to suggest that both genes and prenatal environment influence life chances. However, recent within-twin estimates also raise questions about how the influence of genes and prenatal environment may vary across different subgroups of a population and over time. This paper explores such potential variation within the 1st year of life. Using data on twin births from the 1995-1997 Matched Multiple Birth Database and an analytic strategy based on the Weinberg assumption, this paper considers how associations between birth weight and infant mortality vary across identical and fraternal twins, gestational age, and time. Results suggest that the influence of genes and prenatal environment vary most significantly by gestational age. In pregnancies that lasted less than 37 weeks, within-twin variation in prenatal environment is able to account for negative associations between birth weight and infant mortality. However, in pregnancies that lasted 37 weeks or longer, underlying genetic variation across fraternal twins appears to be largely responsible for birth weight-mortality associations. Such distinct findings by gestation suggest that genes and prenatal environment may play varying roles in birth weight-mortality associations across different situations.

Birth Weight↗